Gastrointestinal bleeding


























Adult patients
Peptic ulcer disease
Erosive gastritis, esophagitis, or duodenitis
Varices (esophageal and gastric)
Portal hypertensive gastropathy
Mallory Weiss tears
Malignancy
Aortoenteric fistula
Pediatric patients
Esophagitis
Gastritis
Peptic ulcer disease




Table 35.2. Common etiologies of LGIB



























Adult patients
Diverticular disease
Vascular ectasia
Ischemic colitis
Hemorrhoids
Inflammatory bowel disease
Malignancy
Meckel’s diverticulum
Pediatric patients
Infectious colitis
Inflammatory/infectious enteritis/colitis
If the patient is under 2 years old, consider Meckel’s diverticulum or intussusception




Presentation


Classic presentation


  • UGIB

    • Patients typically present with hematemesis, coffee-ground emesis, and/or melena.
    • Hematemesis: more easily recognized as “coffee grounds,” usually signifies higher risk of active bleeding.
    • Melena: dark, tarry stools. Usually suggests a minimum loss of 100–200 mL of blood from UGI tract. Dark color is due to the partial digestion of blood and therefore indicates blood that has been present in the GI tract for 12–14 hours.

  • LGIB

    • Patients typically present with bright red blood per rectum (BRBPR), also known as hematochezia.
    • Caveat: large (usually >1 L) or brisk UGIB may present with BRBPR or hematochezia as well. Approximately 10–15% of hematochezia is due to UGIB.

  • In addition, patients may present with symptoms/signs of associated comorbidities (e.g., encephalopathy due to liver disease, dyspnea due to blood loss, etc.).

Critical presentation


  • Higher severity of disease is indicated by:

    • Signs of shock such as hypotension, tachycardia, altered mental status (AMS), decreased urine output (UOP), cool skin, syncope, orthostasis. Change in pulse with posture is more sensitive than hypotension, but may be masked by medications (e.g., beta-blockers).
    • Elderly patient with more than two comorbidities, recurrent hemorrhage, or ischemic chest pain.
    • History of variceal bleed, known liver disease, history of cirrhosis, stigmata of liver disease, excessive alcohol use.
    • Aorto-enteric fistula should be considered if there is a history of aortic graft surgery.
    • The presence of hematemesis, hematochezia in the setting of UGIB is more likely variceal bleed or more significant bleed (both associated with higher mortality).

Diagnosis and evaluation



  • Vital signs

    • Hypotension, tachycardia, and tachypnea can indicate hemorrhagic shock and requires immediate treatment.

  • History

    • Ask about history that may be significant for peptic ulcer disease, liver disease, diverticular disease, use of anticoagulation, aortic surgery, etc.
    • Associated risk factors for peptic ulcer disease:

      • Nonsteroidal anti-inflammatory drugs (NSAIDs), anticoagulants, glucocorticoid, or aspirin use
      • Helicobacter pylori infection
      • Critical illness
      • Gastric acid production.

  • Physical

    • Vital signs as above.
    • Rectal examination: On examination, evaluate for melena, BRBPR, heme-positive test of stool, hemorrhoids.
    • Abdominal examination: ascites, old surgical scars, pain/tenderness suggesting acute abdomen (e.g., rebound and guarding).
    • Other: check for stigmata of liver disease (e.g., encephalopathy, gynecomastia), bruising suggestive of anticoagulant use or thrombocytopenia.

  • Nasogastric aspiration and lavage (controversial due to lack of evidence):

    • Procedure causes many false negative results, as well as false positive results.
    • May not be useful for risk stratification.
    • May be helpful in select patients: e.g., patients with hematochezia or melena only without hematemesis to evaluate for potential UGIB.
    • Risk of use among patients with esophageal varices is unknown.

  • Laboratory testing

    • Complete blood count:

      • Hemoglobin/hematocrit (Hgb/Hct) may not reflect the blood loss during the acute bleeding period.
      • Suspected or confirmed significant blood loss OR ongoing bleeding are indications for transfusion.
      • Initial Hct <30% for UGIB portends worse prognosis.

    • Coagulation profile (PT/PTT/INR):

      • Initial elevated INR from underlying liver disease portends worse outcomes
      • Caveat: Neither coagulation studies nor platelet count reflects the effects of clopidogrel (Plavix) or other new anticoagulants such as dabigatran (Pradaxa) or rivaroxaban (Xarelto).

    • Type and screen/type and cross:

      • For critical and potentially critical patients, be sure to have blood preemptively prepared by the blood bank.

    • Chemistries:

      • BUN/creatinine ratio >30 is suggestive of GI bleed because digested blood is a source of urea.
      • Use chemistries to evaluate for associated comorbidities such as renal failure or liver disease.

    • Cardiac enzymes:

      • Use cardiac enzymes to evaluate for signs of cardiac stress and to evaluate for other etiologies (e.g., abdominal pain could be the only symptom of a myocardial infarction).

  • Glasgow-Blatchford score

    • This score is based on points assigned from the patient’s vital signs, blood analysis results, and clinical presentation.
    • It can be used to help assess which patients may be discharged home with outpatient follow-up. Patients must have all the following criteria to be considered a score of 0 and potentially safe for outpatient follow-up:

      • Normal Hgb (>12.9 g/dL for men, 11.9 g/dL for women)
      • SBP >109 mmHg
      • Pulse <100 beats/minute
      • No melena, syncope, heart failure, or liver failure.

  • Differentiating UGIB from LGIB

    • UGIB is suggested by

      • History of upper GI bleed or peptic ulcer disease risk factors
      • Melanic stool on examination
      • NG lavage with blood or coffee grounds, and BUN/Cr ratio U+226530 (all of these have specificities over 90%, but low sensitivities).

    • LGIB is suggested by

      • History of LGIB, hemorrhoids, diverticular disease
      • Clots in stool
      • Remember, 10–15% of patients presenting with BRBPR have UGIB.

Critical management



  • All patients

    • Large-bore IV access for volume resuscitation: short, large, peripheral IVs. Remember, due to smaller size of lumen and length, multilumen central lines are significantly slower and not the best for volume resuscitation!
    • Secure the airway if indicated.
    • Type and cross for blood products.
    • Transfuse for active bleeding or known low hemoglobin.
    • Correct coagulopathy, thrombocytopenia:

      • Consider indication for the patient’s anticoagulation and weigh the risk of further bleeding before reversing anticoagulation.
      • Consider fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) to reverse warfarin, factor Xa inhibitors, and coagulopathy from liver disease.
      • Consider protamine for patients on heparin.
      • With active bleeding, goal platelet count should be >50 000 cells/microliter.
      • Consider platelet transfusion for patients with dysfunctional platelets (e.g., aspirin/clopidogrel).
      • Consider desmopressin (DDAVP) in the setting of renal failure to help with uremic platelet dysfunction.
      • There are no reversal agents for newer direct thrombin inhibitors.
      • There is no evidence to support use of factor VIIa.
      • Consider antifibrinolytic agents in the setting of massive bleeding.
      • Massive transfusion protocols are helpful for significant bleeding in order to prevent further coagulopathy due to transfusion of high volume of crystalloid or only red cells.

    • Consider consulting GI for emergent endoscopy.
    • Consider admitting to intensive care unit.

  • Management specifics for UGIB

    • Peptic ulcer disease:

      • Consider proton pump inhibitors (PPIs) if there is suspicion for peptic ulcer disease.
      • H2-receptor antagonists have not been shown to have the same reduction in rebleeding or transfusion requirements as PPIs.
      • Consider use of erythromycin to promote gastric motility and help improve visualization during endoscopy.

    • Variceal bleeding:

      • Decrease splanchnic blood flow (limited evidence supporting use):

        • Octreotide: bolus and infusion
        • Vasopressin: bolus and infusion.

      • Prophylactic antibiotics (usually fluoroquinolone or third-generation cephalosporin) to prevent spontaneous bacterial peritonitis due to higher risk of bacterial translocation during acute GIB.
      • Insertion of Blakemore/Minnesota tube to tamponade bleeding varices. Can be used for both gastric and esophageal varices and potentially rectal varices as well.
      • Transjugular intrahepatic portosystemic shunt (TIPS):

        • Placement of stent from portal vein to hepatic vein to decrease pressure in the portal system.
        • Usually placed by the interventional radiology team.
        • Can act as a bridge to liver transplantation in the setting of severe or recurrent bleeding.

  • Management specifics for LGIB

    • There are fewer evidence-based therapies for LGIB than for UGIB.
    • Angiography can identify the site in 40% of LGIB, but must be actively bleeding (usually indicated by unstable vital signs or continued need for transfusion).
    • Consider tagged RBC scan, capsule endoscopy, or push enteroscopy for stable patients.
    • Sigmoidoscopy/colonoscopy is also helpful for stable patients and has the potential benefit of also being therapeutic.
    • Management of LGIB requires surgical intervention more often than UGIB.

Special circumstances



  • Aortoenteric fistula

    • Suggested by a history of aortic graft (at any time).
    • The fistula usually involves the lower duodenum or jejunum.
    • Emergent surgical consultation is needed as esophagogastroduodenoscopy or colonoscopy will not visualize these areas and will not be therapeutic.

  • Liver disease

    • Manage as variceal bleeding.

  • Jehovah’s Witnesses

    • It is unlawful to transfuse if the patient expressly forbids it; document the patient’s wishes carefully.
    • Manage shock and critical illness according to standard protocols.
    • Experimental use of hemoglobin substitutes is not yet approved by the FDA.
    • Most other treatment options (i.e., erythropoietin, factor VIIa) are not helpful in the short term for acute bleeding.
    • Some patients will accept fractions of whole blood (e.g., albumin) or transfusions.

Vasopressor of choice: give blood products (i.e., massive transfusion) first then consider norepinephrine.


References


Alharbi A, Almadi M, Barkun, Martel M. Predictors of a variceal source among patients presenting with upper gastrointestinal bleeding. Can J Gastroenterol. 2012; 26: 187–92.

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Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Gastrointestinal bleeding

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